Hydroxyurea’s efficacy in sickle cell disease is generally attributed to its ability to raise the levels of Hb F in the blood; however, the mechanisms by which it does so are unclear. Early studies suggested that hydroxyurea is cytotoxic to the more rapidly dividing late erythroid precursors, resulting in the recruitment of early erythroid precursors with an increased capacity to produce Hb F. One recent study supports a nitric oxide-derived mechanism for the induction of Hb F by hydroxyurea, and another study suggests that ribonucleotide reductase inhibition is responsible for this increase in Hb F. Alternatively, hydroxyurea may be.
